Abnormal Rich-Club Organization Associated with Compromised Cognitive Function in Patients with Schizophrenia and Their Unaffected Parents

Abnormal Rich-Club Organization Associated with Compromised Cognitive Function in Patients with Schizophrenia and Their Unaffected Parents
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异常的富人俱乐部组织与精神分裂症患者及其未患病父母的认知功能受损相关

DOI:
10.1007/s12264-017-0151-0
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发表时间:
2017-06
影响因子:
5.6
通讯作者:
Zhang D
Zhang D
中科院分区:
医学2区
文献类型:
--
作者:
Zhao Xin;Tian Lin;Yan Jun;Yue Weihua;Yan H;Zhang D

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精神分裂症被认为是一种大脑连接障碍,可能是由富人俱乐部组织不成比例的受损造成的。富人俱乐部由高度互联的中枢区域组成,这些区域在整合不同大脑区域之间的信息方面发挥着至关重要的作用。很少有研究调查患者及其一级亲属的结构性富裕俱乐部组织是否受到损害。在这项研究中,我们使用扩散张量成像建立了19例患者和39名未患病父母、22名年轻健康对照患者和25名老年健康对照父母脑白质联系的加权网络模型。与对照组相比,精神分裂症患者及其未受影响的父母的致富俱乐部结节与非致富俱乐部结节之间的馈线边缘显著减少。此外,在未受影响的父母中,喂食器边缘与类别流畅性测试-动物命名的分数呈显著正相关。特定的饲养层边缘显示出区分未患病父母和老年健康对照的84.4%的准确率。我们的发现表明,富人俱乐部组织受损,特别是支线边缘受损,可能与精神分裂症的家族易感性有关,可能反映了精神分裂症的遗传易感性。
Schizophrenia is considered to be a disorder of brain connectivity, which might result from a disproportionally impaired rich-club organization. The rich-club is composed of highly interconnected hub regions that play crucial roles in integrating information between different brain regions. Few studies have yet investigated whether the structural rich-club organization is impaired in patients and their first-degree relatives. In this study, we established a weighted network model of white matter connections using diffusion tensor imaging of 19 patients and 39 unaffected parents, 22 young healthy controls for the patients, and 25 old healthy controls for the parents. Feeder edges between rich-club nodes and non-rich-club nodes were significantly decreased in both schizophrenic patients and their unaffected parents compared with controls. Furthermore, the feeder edges showed significant positive correlations with the scores in Category Fluency Test—animal naming in the unaffected parents. Specific feeder edges exhibited discriminative power with accuracy of 84.4% in distinguishing unaffected parents from old healthy controls. Our findings suggest that impaired rich-club organization, especially impaired feeder edges, may be related to familial vulnerability to schizophrenia, possibly reflecting a genetic predisposition for schizophrenia.
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